Regulation by sphingolipids of the fate of FRTL-5 cells.
Sphingolipids, including ceramide (Cer), sphingosine (Sph), and sphingosine 1-phosphate (Sph-1-P) have recently emerged as signal-transducing molecules. Functionally, a distinguishing characteristic of these lipids is their apparent participation in pro- or anti-proliferative cell regulation pathways. In this study, we examined the involvement of sphingolipids in the fate of FRTL-5 thyroid follicular cells. We first examined the effects of sphingolipids on FRTL-5 cell viability. Sph and Cer induced apoptosis, as revealed by fluorescence microscopy of TUNEL-positive fragmented nuclei and 180-300 bp DNA fragmentation on agarose gel electrophoresis while Sph-1-P was confirmed to prevent FRTL-5 cell apoptosis induced by deprivation of serum and TSH, possibly via cell surface receptors. We then analysed the metabolism of radiolabelled Sph and C(6)-Cer (a synthetic cell-permeable Cer) in FRTL-5 cells by thin layer chromatography, followed by autoradiography. Sph was mainly metabolized to Cer, and then to sphingomyelin, while Sph conversion into Sph-1-P was hardly detected. These changes were not affected by stimulation of the cells with TSH. Our results indicate the involvement of sphingolipid mediators in the fate of FRTL-5 thyroid cells.
Satoh
Yumiko
Y
Department of Clinical Laboratory, The University of Tokyo Hospital, Tokyo, Japan.
Li
Xin
X
Yokota
Hiromitsu
H
Osada
Makoto
M
Ozaki
Yukio
Y
Katoh
Ryohei
R
Yatomi
Yutaka
Y
D000818:Animals; D016923:Cell Death; D002470:Cell Survival; D002478:Cells, Cultured; D002518:Ceramides / Q000378:metabolism; D008246:Lysophospholipids / Q000378:metabolism; D051381:Rats; D011956:Receptors, Cell Surface / Q000378:metabolism; D013107:Sphingolipids / Q000378:metabolism*; D013110:Sphingosine / Q000031:analogs & derivatives / Q000378:metabolism
D002518:Ceramides; D008246:Lysophospholipids; D011956:Receptors, Cell Surface; D013107:Sphingolipids; C060506:sphingosine 1-phosphate; D013110:Sphingosine